The pathway was discovered accidentally by two separate research groups, both investigating genes related to physiological development.

"We were trying to make mouse models of Lin28-driven cancer, but we were surprised to find that these mice had super long tails," researcher George Daley, dean at Harvard Medical School, said in a news release. "They had more vertebrae."

Daley and his colleagues were studying the Lin28/let-7 pathway, a series of genes that regulates developmental timing. The path has been linked with several cancers.

Researchers in Portugal found Gdf11, a gene that controls embryonic development of the tail in mice, finding during lab tests that Gfd11 mutations caused mice to grow shorter, thicker tails.

"They also contained a fully grown neural tube inside, as opposed to a normal tail that is essentially made of vertebrae," said Moises Mallo, researcher at the Instituto Gulbenkian de Ciência in Portugal.

Both teams of scientists inadvertently showcased the primary role the gene Lin28 plays in tail development.

"We were able to pinpoint the Lin28 and Hox13 genes as key regulators of tail development downstream from Gdf11," Mallo said.

Both Lin28 and Hox13 control the deployment of somites, blocks of cells that transform into specialized cell types, forming dermis, skeletal muscle, cartilage, tendons and vertebrae.

"From my perspective, one of the most important findings of our work is that a group of multipotent cells that build both the somites and the spinal cord are regulated by fundamentally different genetic networks and have different cell competences at two consecutive stages of development," Mallo said. "This finding goes beyond the trunk to tail transition, possibly acquiring relevance in pathological processes like the initiation of metastasis."

"Anterior-posterior axis elongation is an important feature in bilateral animals, and natural selection has created a variety of tail lengths to suit different evolutionary pressures," said Harvard researcher Daisy Robinton. "Until now, little was known about how length is controlled and how the manipulation of genetics can impact morphogenesis."